Evidence map›Paper›PMID 30692699›Full record

ArticleNature medicine2019

ApoE attenuates unresolvable inflammation by complex formation with activated C1q.

Changjun Yin, Susanne Ackermann, Zhe Ma, Sarajo K Mohanta, Chuankai Zhang, Yuanfang Li, Sandor Nietzsche, Martin Westermann, Li Peng, Desheng Hu and 19 more

Erratum issuedOpen access · greenAbstract readVideo-Audio Media
In one paragraph

Article in Nature medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 178 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
178citing papers in PubMed, 1 pooled it
20.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

178 citing papers in PubMed, 1 synthesis or guideline pooled it, 308 citations in OpenAlex.

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  16. CD80Cell communication and signaling : CCS · 2026
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118 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

29 authors at 12 institutions in 5 countries.

Changjun YinInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany. changjun.yin@med.uni-muenchen.de.ORCID http://orcid.org/0000-0002-1913-4477
Susanne AckermannLeibniz Institute for Natural Product Research and Infection Biology, Jena, Germany.ORCID http://orcid.org/0000-0001-8179-5201
Zhe MaInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany.
Sarajo K MohantaInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany.ORCID http://orcid.org/0000-0001-6144-4092
Chuankai ZhangInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany.
Yuanfang LiInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany.
Sandor NietzscheCentre for Electron Microscopy, Jena University Hospital, Friedrich-Schiller-University of Jena, Jena, Germany.
Martin WestermannCentre for Electron Microscopy, Jena University Hospital, Friedrich-Schiller-University of Jena, Jena, Germany.
Li PengDepartment of Cardiovascular Medicine of Second Affiliated Hospital, Guizhou University of Traditional Chinese Medicine, Guiyang, China.
Desheng HuDepartment of Integrated Traditional Chinese and Western Medicine, Union Hospital, Huazhong University of Science and Technology, Wuhan, China.
Sai Vineela BonthaDepartment of Surgery, University of Tennessee, Memphis, TN, USA.ORCID http://orcid.org/0000-0001-8914-1966
Prasad SrikakulapuCardiovascular Research Center (CVRC), University of Virginia, Charlottesville, VA, USA.
Michael BeerDepartment of Information Technology, University Clinic Jena, Jena, Germany.
Remco T A MegensInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany.
Sabine SteffensInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany.
Markus HildnerInstitute for Anatomy II, University Clinic Jena, Jena, Germany.
Luke D HalderLeibniz Institute for Natural Product Research and Infection Biology, Jena, Germany.
Hans-Henning EcksteinDepartment for Vascular and Endovascular Surgery, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Jaroslav PelisekDepartment for Vascular and Endovascular Surgery, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Jochen HermsCenter for Neuropathology and Prion Research, Ludwig-Maximilians-University, Munich, Germany.
Sigrun RoeberCenter for Neuropathology and Prion Research, Ludwig-Maximilians-University, Munich, Germany.
Thomas ArzbergerCenter for Neuropathology and Prion Research, Ludwig-Maximilians-University, Munich, Germany.
Anna BorodovskyAlnylam Pharmaceuticals Cambridge, Cambridge, MA, USA.
Livia HabenichtII. Medizinische Klinik und Poliklinik, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Christoph J BinderDepartment of Laboratory Medicine, Medical University of Vienna and Center for Molecular Medicine (CeMM) of the Austrian Academy of Sciences, Vienna, Austria.
Christian WeberInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany.ORCID http://orcid.org/0000-0003-4610-8714
Peter F ZipfelLeibniz Institute for Natural Product Research and Infection Biology, Jena, Germany.ORCID http://orcid.org/0000-0002-6149-2411
Christine SkerkaLeibniz Institute for Natural Product Research and Infection Biology, Jena, Germany. christine.skerka@hki-jena.de.ORCID http://orcid.org/0000-0003-2374-6473
Andreas J R HabenichtInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany.ORCID http://orcid.org/0000-0003-2901-3027
Ludwig-Maximilians-Universität München · DEJena University Hospital · DELeibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DETUM Klinikum · DEGerman Centre for Cardiovascular Research · DEMaastricht University · NLAlnylam Pharmaceuticals (United States) · USAustrian Academy of Sciences · ATMunich Cluster for Systems Neurology · DEUnion Hospital · CNUniversity of Tennessee Health Science Center · USUniversity of Virginia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apolipoprotein-E (ApoE) has been implicated in Alzheimer's disease, atherosclerosis, and other unresolvable inflammatory conditions but a common mechanism of action remains elusive. We found in ApoE-deficient mice that oxidized lipids activated the classical complement cascade (CCC), resulting in leukocyte infiltration of the choroid plexus (ChP). All human ApoE isoforms attenuated CCC activity via high-affinity binding to the activated CCC-initiating C1q protein (K

Indexed as

AgedAged, 80 and overAmyloid beta-PeptidesAnimalsAntigen-Antibody ComplexAortaApolipoproteins EAtherosclerosisBrainCarotid ArteriesCarotid Artery DiseasesChoroid PlexusCognitive DysfunctionComplement C1qComplement C5Complement Pathway, ClassicalAmyloid beta-PeptidesAntigen-Antibody ComplexApoE protein, humanApolipoproteins EComplement C1qComplement C5Protein IsoformsRNA, Small Interfering

Identifiers

PMID30692699
PMCPMC6420126
OpenAlexW2911553777

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.